cGMP is an important intracellular messenger and is known to be involved in the regulation of various physiological phenomena such as relaxation and proliferation of smooth muscle cells, aggregation and adhesion of platelets, and signaling of nerve cells, through the control of a cGMP-dependent protein kinase, a phosphodiesterase, and ion channels. The cGMP is catalytically produced from guanosine triphosphate (GTP) by a guanylate cyclase in the response to various extracellular and intracellular stimulation. There have been reported two groups of guanylate cyclases to date, that is, particulate guanylate cyclases stimulated by peptidic messengers (for example, atrial natriuretic peptides, brain natriuretic peptides, and the like) and sGC stimulated by nitric oxide (NO).
With respect to the sGC, the following are known. That is, the sGC is one of the most important target molecules of NO that is a messenger which plays a very important role in maintaining homeostasis of the body, and forms an NO/sGC/cGMP pathway. It has been reported that this enzyme is constituted with two subunits, each of the heterodimer contains one heme, and the heme plays a central role in an activation mechanism. It is believed that when NO binds to the iron atom in the heme, the enzyme is changed to an active conformation. Therefore, there is no stimulation by NO with enzyme preparations containing no heme. Although carbon monoxide (CO) may also bind to the iron in the heme, but the stimulation by CO is significantly lower than that by NO.
The sGC is constituted with α and β subunits. Analysis of sGC from tissue-specific distributions and in different growth steps demonstrated multiple subtype with different subunit compositions. The distribution of the respective subunits have been studied with mammals including a human, and it has been widely known that α1 and β1 subunits are expressed in many tissues and the α1β1 forms have a pattern of a heterodimer that works functionally. α2 subunits have been also recognised, which exist fewer organs as compared to the α1. It has been reported that the α2 subunits are expressed more frequently than α1 in the brain, the lung, the colon, the heart, the spleen, the uterus, and the placenta. Subunits called α3 and β3 were isolated from the human brain, but are homologous to α1 and β1. In addition, according to recent studies, α2i subunits which contain an insert in the catalytic domain have identified. All of these subunits exhibit high homology in catalytic domain regions.
Under pathophysiological conditions, such as hyperglycemia, hyperlipidemia, hypertension, or the like, it has been reported that there is inhibition of the production of or promotion of the degradation of sGC activating factors such as NO for the reasons of increased generation of free radicals, and the like. With a decrease in the sGC activating factors, NO/sGC/cGMP signals are attenuated, which causes, for example, increased blood pressure, platelet activation, or increased cell proliferation and cell adhesion. As a result, a variety of cardiovascular diseases, specifically, hypertension (including pulmonary hypertension), atherosclerosis, lumbar spinal canal stenosis, peripheral arterial diseases, intermittent claudication, critical limb ischemia, stable or unstable angina pectoris, heart failure, thrombosis, stroke, sexual dysfunction, and the like occur. Therefore, a new drug having a mechanism of activating sGC is expected to be useful for treating or preventing such diseases by normalizing cGMP production.
As the sGC activator, there have been known, for example, “heme-dependent activators” which activate sGC depending on heme groups, such as NO donors as described later and the like, and “heme-independent activators” which are independent on the heme groups (Non-Patent Document 1).
For the activation of sGC, a group of compounds called NO donors such as organic nitrates have been widely used so far. These compounds are heme-dependent activators which activate sGC by being metabolized in vivo to produce NO, which then binds to a central iron atom of a heme. However, the NO donors have critical disadvantages such as expression of a resistance, a decrease in the effects and the like is expressed in addition to side-effects, and therefore, there is a demand for a novel sGC activator that does not have these disadvantages.
For example, compounds of the following formulae (a) to (c) have been reported as compounds having sGC activating action (Patent Document 1).

(Compounds of the formula (a) are pyrazolo[3,4]fused bicyclic compounds, and compounds of formulae (b) and (c) are imidazo[1,5]fused bicyclic compounds. Further, Q means substituted heterocycle in any one of the formulae (a) to (c). For details, refer to the document.)
In this document, there is no disclosure or suggestion of compounds having an imidazo[1,2-a]pyridine scaffold.
In addition, pyrazole derivatives or pyrazolo[3,4-b]pyridine derivatives are disclosed as the sGC activating compounds in International Publications WO 2000/06569, WO 2000/21954, WO 2001/83490, WO 2003/004503, WO 2003/095451, WO 2003/086407, WO 2003/097063, WO 2007/124854, WO 2007/128454, WO 2008/031513, WO 2008/061657, WO 2010/078900, WO 2010/079120, WO 2011/147809, WO 2012/004258, WO 2012/004259, WO 2012/010576, WO 2012/010577, WO 2012/010578, WO 2012/028647, WO 2012/059548, WO 2012/059549, WO 2012/143510, WO 2012/152629, WO 2012/152630, WO 2013/004785, WO 2013/030288, WO 2013/104597, WO 2013/104598, and WO 2013/104703. However, in any of these documents, there is no disclosure or suggestion of compounds having an imidazo[1,2-a]pyridine scaffold.
Furthermore, compounds of the following formula (d) have been reported as sGC activators (Patent Document 2).

(wherein Z is O, S, or N(R7), R7 is H or alkyl, and R6 is aryl, arylalkenyl, heteroring, -(alkenyl)-(heteroring), or heterocycloalkyl. For details, refer to the document).
However, this document does not disclose or suggest compounds having an imidazo[1,2-a]pyridine scaffold.
As other sGC activators, 1H-pyrazole-5-carboxylic acid derivatives (Patent Document 3), biaryl derivatives (Patent Document 4), and benzylindazole derivatives (Non-Patent Document 2) have been reported.
Furthermore, compounds having an imidazo[1,2-a]pyridine scaffold, for example, compounds of the following formula (e) useful for the treatment of gastrointestinal ulcer as an H+/K+-ATPase inhibitors have been reported (Non-Patent Document 3).

(wherein R means substituted alkoxy group, R′ means H or phenethyl, R2 means H or lower alkyl, and R3 means substituted alkyl or the like. For details, refer to the document).
This document does not disclose or suggest sGC activators, and aminocarbonyl is not included in R3 of the compound of the formula (e).
Moreover, compounds of the formula (f) useful for the treatment of allergy, inflammation, pain, or the like as bradykinin antagonists have been reported (Patent Document 5).

(wherein R1 to R3 each mean hydrogen, lower alkyl, or the like, R4 means an aryl group which may have a suitable substituent, or the like, Q means O, NH, or the like, X1 means N or C—R5, Y1 and Y2 each mean a single bond or a lower alkylene group, and Ring A means 6-membered nitrogen-containing heterocycle. For details, refer to the document).
This document does not disclose or suggest sGC activators, and aminocarbonyl is not included in R1 of the compound of the formula (f).
Furthermore, compounds of formula (g) with H+/K+-ATPase enzyme inhibitory activities and useful for the inhibition of gastric acid secretion have been reported (Patent Document 6).

(wherein R1 is CH3 or CH2OH, R2 and R3 are each lower alkyl, R4 is H or halogen, R5 is H, halogen, or lower alkyl, and X is NH or O. For details, refer to the document).
This document does not disclose or suggest sGC activators, and aminocarbonyl is not included in R1 of the compound of the formula (g).
Moreover, compounds of formula (h) have been reported as cardiac ion channel modulators and as antiarrhythmic agents (Patent Document 7).

(wherein R2, R15, R16, and R18 are each Br, Cl, F, carboxy, H, —OH, hydroxymethyl, or the like, and R1 is H, C1-6 alkyl, aryl, benzyl, or the like. For details, refer to the document).
This document does not disclose or suggest sGC activators, and aminocarbonyl is not included in R16 of the compound of the formula (h).
In addition, compounds of formula (i) useful as a drug for treating bacterial infection, particularly tuberculosis, have been reported (Patent Document 8).

(wherein X, Y, and Z are each CH or the like, n is 0 to 3, m is 0 to 4, R1 is —C(O)N(R4)2 or the like, R2 is C1-10 alkyl or the like, R3 is —OR6 or the like, and R6 is C1-10 alkyl optionally substituted, or the like. For details, refer to the document).
This document specifically discloses a compound, in which X, Y, and Z are each CH, n is 0, R1 is —C(O)N(R4)2, R2 is C1-10 alkyl, m is 1, R3 is —OR6, and R6 is H, methyl, or difluoromethyl. However, this document does not disclose or suggest sGC activators.
In addition, compounds of formula (j) with sGC activity and useful for cardiovascular diseases, in particular intermittent claudication and critical limb ischemia accompanied with peripheral arterial diseases as well as hypertension, and the like, have been reported (Patent Document 9).

(wherein A1 is cycloalkyl which may be substituted, aryl which may be substituted or the like, R1 is H or the like, R2 is R0 or the like, R0 is lower alkyl, R3 is H or the like, R4 is —Y-A2 or the like, Y is C1-10 alkylene which may be substituted or the like, and A2 is heteroaryl which may be substituted. For details, refer to the document).